During the periparturient period, the abrupt increase in energy demand for milk production induces metabolic disorders. Our previous work has shown that reducing milk output by milking once a day or partially in the first days of lactation reduces these disorders. The aim of this study was to reduce metabolic disorders by limiting milk production during the first week of lactation through inhibition of the lactogenic signal driven by prolactin. Twenty-two late gestation cows were assigned into 2 groups based on parity and milk production of the first 100 d of the previous lactation. Both groups received 8 i.m. injections of either quinagolide (Quin; 2mg of an inhibitor of prolactin release) or water (CTL) just after calving, and the subsequent 7 injections were given every 12h. Milk production was measured until d 28 post-calving. Blood samples were taken from d 1 (calving) to 5 and then on d 7, 10, 14, 21 and 28 to measure concentrations of urea, phosphorus, calcium, glucose, nonesterified fatty acids (NEFA), β-hydroxybutyrate and prolactin (PRL). Prolactin concentrations were lower (P < 0.01) in Quin cows from d 2 to d 5. Interestingly, between d 10 and d 28, PRL concentrations were greater (P < 0.05) in Quin than CTL cows. Milk production was lower in Quin cows from d 2 to d 6 than in control (24.3 ± 6.4 kg/d vs 34.8 ± 4.1 kg/d; P < 0.05). There was no residual effect of quinagolide on milk production after d 6. The blood glucose and calcium concentrations were greater (P < 0.05) in Quin cows whereas the concentration of β-hydroxybutyrate was greater (P < 0.05) in CTL cows during the first week of lactation. Blood NEFA, urea and phosphorus were not affected by treatment. In conclusion, reducing the prolactin peak at calving is effective to reduce milk production during the first week of lactation without compromising the global productivity of the dairy cow. This reduction in milk production allows a reduction of the metabolic stress during this period.